[2003]Dissection of the Aorta a New Approach

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    Dissection of the aorta: a new approachM Mikich. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

    Heart2003;89:68

    There are two generally proposed causes of dissectionof the aorta: (1) cleavage caused by blood entering thetear; and (2) haemorrhage that dissects the media andtear secondary to the cleavage. Using analysis ofpressures and forces, this article shows that, on someoccasions, these mechanisms alone cannot beresponsible for causing aortic dissection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

    This article addresses a possible cause ofdissection of the aorta. Let us start with a

    variation of dissection which is not socommonthat is,the dissection that has an entrytear located just beyond the left subclavian artery,but which extends proximally into the ascendingaorta (in other words, the dissection cleavagepropagates from the tear towards the aorticroot).1 2

    To simplify matters,let us assume that the bodyis in the supine position. In other positions of thebody the calculation is a bit more complicated butthe result is the same.

    ANALYSIS OF PRESSURES AND FORCESForces acting on the flap proximally fromthe tearIt is thought that cleavage from blood entering

    through the tear causes the propagation of

    dissection towards the aortic root. This is repre-

    sented in fig 1. Points denoted with F are in the

    false channel and those denoted as T are in the

    true channel. If we compare pressure in the true

    channel at the tear to pressure at the aortic root it

    is obvious that pressure in the true channel

    always gradually rises from the tear to the aortic

    root (so pressure at T1 is greater than pressure at

    the tear, pressure at T2 is greater than pressure at

    T1, and pressure at T3 is greater than at T2).

    If there is no flow in the false channel the pres-sure at any point within the false channel must bethe same as the pressure at the tear (so pressure

    at F0, F1, F2, and F3 is the same as at the tear).

    When applying these facts to fig 1 it is obviousthat pressure at point T1 is greater than the pres-

    sure at point F1, that pressure at T2 is greater than

    pressure at F2, and that pressure at T3 is greaterthan pressure at F3. This means that the pressure

    difference pushes the flap towards the adventitia.

    Therefore, cleavage by blood from the tear cannotbe the cause of propagation of dissection from the

    tear towards the aortic root. This is true no matter

    how close the tear is to the aortic root. Even if the

    tear is just above the aortic root (as in type I) it isobvious that the cleavage caused by blood from

    the tear cannot undermine the aortic valve.

    If blood enters from the true channel throughthe tear into the false channel (that is, flows

    towards point F3) then pressure at F1 is lower

    than pressure at the tear (because liquid can flow

    only from higher pressure towards lower pres-

    sure), pressure at F2 is lower than at F1, and

    pressure at F3 is lower than at F2. Therefore, the

    pressure difference that pushes the flap towards

    the adventitia is greater than in the case in which

    there is no flow in the false channel.

    Pressure drop in the aortaTo calculate maximum forces acting on the flap,

    the maximum pressure difference between a

    point in the false channel and its most adjacentpoint in the true channel (for instance, between

    the points F0 and T0) must be determined. The

    maximum pressure difference is when there is

    maximum pressure drop along the aorta. Since

    the maximum pressure at the aortic root is systo-

    lic and minimum pressure at the distal end of the

    aorta is diastolic, the maximum pressure differ-

    ence between the aortic root and distal end

    cannot be greater than systolic pressure minus

    diastolic pressure. It can also be assumed that

    pressure linearly falls from the aortic root to the

    distal end.

    So if, for example, systolic pressure is

    135 mm Hg, diastolic pressure is 90 mm Hg, andthe length of the aorta is 45 cm, then the

    maximum pressure drop is (135 90)/45 =1 mm Hg/cm (this pressure drop will be used in

    further calculations).

    Forces acting on the flap distally from tearIf the distance between the tear and T0 (fig 1) is

    1 cm then pressure at T0 is 1 mm Hg lower than

    at the tear. When there is no flow in the false

    Figure 1 Calculation of forces that act on the flap.Point F0 is just at the distal end of the dissection.

    . . . . . . . . . . . . . . . . . . . . . . .

    Correspondence to:Mr Boris Mikich, FranaAlfirevica 29, 10000Zagreb, Croatia;[email protected]. . . . . . . . . . . . . . . . . . . . . . .

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    channel, the pressure at F0 (point F0 is just at the distal endof the false channel) is equal to the pressure at the tear, so the

    pressure at F0 is 1 mm Hg higher than at T0. Since the

    pressure difference at the beginning of the flap (just at the

    tear) is zero, the mean pressure difference on the flap distally

    from the tear is (0 + 1)/2 = 0.5 mm Hg. If we suppose, for the

    purpose of this discussion, that the transverse length of the

    flap is 5 cm (longitudinal length is equal to distance between

    tear and F0 or T0that is, 1 cm) then the area of the flap dis-

    tal to the tear is 5 1 cm2which, when multiplied by the meanpressure difference on the flap, gives a force by which the flap

    distal to the tear is pushed towards the true channel.

    Converting 0.5 mm Hg to N/m2 gives (1 mmHg = 132.88

    N/m2 at 20C): 0.5 132.88 = 66.4 N/m2, and converting cen-

    timetres to metres 1 cm = 0.01 m and 5 cm = 0.05 m. Thus,the force is:

    66.4 0.01 0.05 = 0.0332 N.

    This force is too small to cause any further increase of the

    dissection in the distal direction. If blood enters the false

    channel then the pressure at F0 is lower than in the case when

    there is no flow in the false channel, therefore forces on the

    flap are lower too.

    Forces from haemorrhageIt is also thought that haemorrhage dissects the media and

    that tear is secondary to it. Figure 2 shows a haemorrhage in

    the media. Point T is the point in the lumen of the aorta whichis nearest to the haematoma. For the purpose of this

    discussion, let us say that the haemorrhage is situated just

    beyond the left subclavian artery, about 15 cm from the aortic

    root. If we use the same pressure drop as in the previous

    example, then pressure at point T is 15 cm 1 mm Hg/cm =15 mm Hg lower than at the aortic root. The maximum possi-

    ble pressure in the haematoma is pressure at the aortic root.

    This means that pressure in the haematoma cannot be more

    than 15 mm Hg higher than at point T and from that the

    maximum force produced by the pressure difference between

    the haematoma and point T can be calculated.

    Let us suppose that the haematoma has an area of 2 2 mm.Converting 15 mm Hg to N/m2 gives: 15 132.88 = 1993 N/m2,

    and converting millimetres to metres, 2 mm = 0.002 m. Thus,the maximum force that is produced by the pressure

    difference between the haematoma and T is:

    1993 0.002 0.002 = 0.00797 N.

    That force is too small to make any cleavage in the media orto tear the intima. If there is haemorrhage at the aortic root

    then the pressure difference between the haematoma and the

    most adjacent point to it in the lumen of the aorta is zero;

    therefore it is obvious that there is no force at all and that

    blood from that haematoma cannot undermine the aortic

    valve.

    THE REAL CAUSE OF DISSECTIONFormation of the dissectionIf the aortic smooth muscles contract the adventitia will

    follow that contraction. But as seen in fig 3, at the area of the

    aorta where the left subclavian, left carotid, and brachio-

    cephalic artery originate, downward movement of the aortic

    wall is very limited by those arteries. Upward movement of

    area A of the aorta is very limited by area D of the aorta. So at

    the segment of the aorta which comprises the origin of the left

    subclavian artery and area A, the aortic wall is fixed at the

    upper and the lower part, so at the upper and lower part of the

    segment the adventitia can only partially follow the contrac-

    tion of smooth muscles (fig 4). As a consequence high stresses

    Figure 2 Calculation of forces that act from the haemorrhage inthe media

    Figure 3 Limitation of upwardmovement of area A by area D.

    Figure 4 Forces Fs from smooth muscles cause stresses in themedia.

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    develop in the media in that segment. If too strong a contrac-

    tion of smooth muscles (spasm) occurs, dissection of the

    media will take place, especially if there are areas of cystic

    degeneration in the media and/or if there is any other

    weakness in the media.

    Why does dissection take place just beyond the origin of the

    left subclavian artery and not at area A? It is because the

    smooth muscles of the aorta (and thus also forces from the

    smooth muscles) are not arranged around the originof the left

    subclavian artery as evenly as they are at area A. This uneven

    distribution causes the concentration of forces in the aortic

    media at the origin of the left subclavian artery which then

    causes dissection.

    Eventually, if the forces from the smooth muscles continue

    to increase, the intima and part of the media on the smooth

    muscle will break and a tear will result.

    Propagation of dissectionFigure 5 shows a transverse cross section of dissection through

    the flap. It can be seen that blood pressure forces act on all the

    inside surfaces of the false and true channels. Assuming, for

    simplicitys sake, that pressures both in the true and in the

    false channel are the same, the forces acting on the flap from

    the false channel and from the true channel are also equal(and so cancel each other) and therefore they are not shown.

    The forces shown stretch the aortic wall. While stretching,

    the aortic wall stretches the flap in the direction that is

    perpendicular to the long axis of the aorta and parallel with

    the flap. Because each force must have a counter force of the

    same intensity and opposite direction it means that the flap

    pulls the aortic wall by force Ff (fig 5, right). That force is

    caused by elasticity of the flap and/or the presence of forces

    from smooth muscles in the flap. This force Ff by which the

    flap pulls the aortic wall tends to damage the media further

    and to increase dissection in the transverse direction. The

    increasing dissection in the transverse direction is accompa-

    nied by movement of the flap towards the centre of the aorta.

    This movement pulls the rest of the flap which is located dis-tally and/or proximally from the part of the flap shown in cross

    section, and that causes further dissection in the distal and/or

    proximal direction.

    If blood pressure rises the stretching of the flap increases;

    consequently the forces that tend to damage the media and to

    increase dissection also rise. Once the flap, which is

    perpendicular to the long axis of the aorta, reaches a certain

    length (the length depending on pressure in the aorta), the

    elastic forces from the flap alone are sufficient to increase dis-

    section further.

    If a tear does not occur, blood from haemorrhage could

    slowly fill the false channel, thus establishing in the false

    channel the same pressure as in the aorta, as occurs when

    there is a tear. But, because of low inflow of blood from haem-orrhage in this case, dissection can propagate only very slowly.

    CONCLUSIONDissection takes place as a consequence of major contraction

    of the smooth muscles, especially when there are areas of

    cystic degeneration in the media, and haemorrhage takes

    place because of dissection of the media. Administration ofblockers and/or calcium antagonists will reduce this strong

    contraction of the smooth muscles, thus reducing dissection.3

    On the other hand, discontinuation of long term therapy with

    blockers may provoke dissection.4

    Fibrous tissue at the aortic root also fixes the aortic wall,

    which makes this part of the aorta also suitable for initiating

    dissection. This fixing of the aortic wall explains why morethan 95% of dissections begin at two places: either just above

    the aortic valve or just beyond the origin of the left subclavian

    artery.5

    In hypertensives there is an increase in smooth muscle

    mass and that also produces a stronger force.6 7 That, together

    with acquired cystic degeneration in hypertensives, mayexplain why dissection takes place mostly in hypertensives.

    Smooth muscles in the media in large, elastic arteries are

    generally helically oriented.8 Therefore it is readily possiblethat dissection propagates in a direction perpendicular to the

    orientation of these helically oriented smooth muscles

    (analogous to normal propagation which is perpendicular tocircumferentially oriented smooth muscles). As a result spiral

    dissection develops, known as spiral barber pole dissection.1

    REFERENCES1 Schlant RC, Alexander RW.Hursts the heart, 8th edn. New York:

    McGraw-Hill, 1994:2170.2 Hurst JW, Alpert JS.Diagnostic atlas of the heart. New York: Raven

    Press, 1994:337.3 Hoshino T, Ohmae M, Sakai A. Spontaneous resolution of a dissection

    of the descending aorta after medical treatment with a beta blocker anda calcium antagonist.Br Heart J1987;58:824.

    4 Eber B, Tscheliessnigg KH, Anelli-Monti M,et al.Aortic dissection due todiscontinuation of beta-blocker therapy.Cardiology1993;83:12831.

    5 Hurst JW, Alpert JS.Diagnostic atlas of the heart. New York: RavenPress, 1994:338.

    6 Owens GK, Schwartz SM. Alterations in vascular smooth muscle mass inthe spontanteneously hypertensive rat. Role in cellular hypertrophy,hyperploidy and hyperplasia.Circ Res1982;51:2809.

    7 Owens GK, Schwartz SM. Vascular smooth muscle cell hypertrophy andhyperploidy in the Goldblatt hypertensive rat. Circ Res1983;53:491501.

    8 Schlant RC,Alexander RW. Hursts the heart, 8th ed. New York:McGraw-Hill, 1994:31.

    Figure 5 Transverse (perpendicular to the long axis of the aorta)cross section of a dissection. The left and right cross sections areidentical, but in the right cross section the flap is not present so thatforces Ff can be shown. Forces from blood pressure acting on theflap from the false channel and the true channel are equal andcancel each other, and therefore they are not shown. Fp, forces fromblood pressure in the aorta; Ff, forces with which the flap pulls theaortic wall.

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